Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/34278
Title: ATP-dependent potassium channel blockade strengthens microglial neuroprotection after hypoxia-ischemia in rats.
Author: Ortega González, Fco. Javier
Gimeno-Bayon, Javier
Espinosa-Parrilla, J.F.
Carrasco Jordan, Josep Lluís
Batlle, M.
Pugliese, Marco
Mahy Gehenne, Josette Nicole
Rodríguez Allué, Manuel José
Keywords: Micròglia
Canals de potassi
Isquèmia cerebral
Lesions cerebrals
Microglia
Potassium channels
Cerebral ischemia
Brain damage
Issue Date: 24-Feb-2012
Publisher: Elsevier
Abstract: Stroke causes CNS injury associated with strong fast microglial activation as part of the inflammatory response. In rat models of stroke, sulphonylurea receptor blockade with glibenclamide reduced cerebral edema and infarct volume. We postulated that glibenclamide administered during the early stages of stroke might foster neuroprotective microglial activity through ATP-sensitive potassium (KATP) channel blockade. We found in vitro that BV2 cell line showed upregulated expression of KATP channel subunits in response to pro-inflammatory signals and that glibenclamide increases the reactive morphology of microglia, phagocytic capacity and TNFα release. Moreover, glibenclamide administered to rats 6, 12 and 24 h after transient Middle Cerebral Artery occlusion improved neurological outcome and preserved neurons in the lesioned core three days after reperfusion. Immunohistochemistry with specific markers to neuron, astroglia, microglia and lymphocytes showed that resident amoeboid microglia are the main cell population in that necrotic zone. These reactive microglial cells express SUR1, SUR2B and Kir6.2 proteins that assemble in functional KATP channels. These findings provide that evidence for the key role of KATP channels in the control of microglial reactivity are consistent with a microglial effect of glibenclamide into the ischemic brain and suggest a neuroprotective role of microglia in the early stages of stroke.
Note: Versió postprint del document publicat a: http://dx.doi.org/10.1016/j.expneurol.2012.02.010
It is part of: Experimental Neurology, 2012, vol. 235, num. 1, p. 282-296
Related resource: http://dx.doi.org/10.1016/j.expneurol.2012.02.010
URI: http://hdl.handle.net/2445/34278
ISSN: 0014-4886
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

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